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PubMed1998

Reappearance of activity in the vestibular neurones of labyrinthectomized guinea-pigs is not delayed by cycloheximide.

1. In mammals, unilateral labyrinthectomy induces an immediate depression of the resting discharges in the neurones of the ipsilateral vestibular nuclei. Later on, a spontaneous restoration of this activity occurs. The aim of the present study was to test the possibility that protein synthesis could be involved in the start of this process in the guinea-pig. 2. Cycloheximide (CHX), a protein synthesis inhibitor, was injected intramuscularly 1 h before (30 mg kg-1) and 5 h after (15 mg kg-1) labyrinthectomy. 3. In a first group of animals, CHX was found to induce an inhibition of protein synthesis at levels ranging from 71 to 93% for 9 h after labyrinthectomy. 4. In a second group of alert animals, we studied single unit activity of second-order vestibular neurones. It was found that, in the 12-16 h post-labyrinthectomy period, at a time when restoration began in guinea-pigs not treated with CHX, the discharges in the labyrinthectomized group treated with CHX were not different from those observed in a previous study in labyrinthectomized animals not treated with CHX. 5. We conclude that protein synthesis is not required for the start of restoration of activity in the vestibular neurones deprived of their ipsilateral labyrinthine input.

Animals↗
PubMed1987

Increased fucosylation of chick brain proteins following training: effects of cycloheximide.

When chicks are trained to avoid pecking a bead coated with methylanthranilate in a one-trial passive avoidance task there is an increase in fucose incorporation in vivo and in vitro in the right forebrain base of methylanthranilate (M)-trained compared to water (W)-trained chicks. The relation of this increase to de novo protein synthesis in vivo and in vitro has been examined. Cycloheximide (Cx), 1 mM, inhibited in vitro fucosylation of chick brain slices by 60% after 3 h. However, the training-related increase in in vitro fucosylation still persisted. When Cx was injected intraventricularly 10 min before training, the subsequent increase in in vitro fucosylation due to training was still apparent. When Cx was injected and [14C]leucine and [3H]fucose incorporation studied in vivo in M-trained and W-trained chicks, there was no increase in fucosylation due to training in the Cx-treated M-trained over the W-trained chicks. These results are taken to indicate that in vitro fucosylation and its increase subsequent to training is not protein synthesis-dependent, but that both in vivo and in vitro there are interactions between Cx and fucosylation steps that are independent of Cx's effects on protein synthesis.

Animals↗
PubMed2005

Growth-associated protein 43 expression in hippocampal molecular layer of chronic epileptic rats treated with cycloheximide.

PURPOSE: GAP43 has been thought to be linked with mossy fiber sprouting (MFS) in various experimental models of epilepsy. To investigate how GAP43 expression (GAP43-ir) correlates with MFS, we assessed the intensity (densitometry) and extension (width) of GAP43-ir in the inner molecular layer of the dentate gyrus (IML) of rats subject to status epilepticus induced by pilocarpine (Pilo), previously injected or not with cycloheximide (CHX), which has been shown to inhibit MFS. METHODS: CHX was injected before the Pilo injection in adult Wistar rats. The Pilo group was injected with the same drugs, except for CHX. Animals were killed between 30 and 60 days later, and brain sections were processed for GAP43 immunohistochemistry. RESULTS: Densitometry showed no significant difference regarding GAP43-ir in the IML between Pilo, CHX+Pilo, and control groups. However, the results of the width of the GAP43-ir band in the IML showed that CHX+Pilo and control animals had a significantly larger band (p = 0.03) as compared with that in the Pilo group. CONCLUSIONS: Our current finding that animals in the CHX+Pilo group have a GAP43-ir band in the IML, similar to that of controls, reinforces prior data on the blockade of MFS in these animals. The change in GAP43-ir present in Pilo-treated animals was a thinning of the band to a very narrow layer just above the granule cell layer that is likely to be associated with the loss of hilar cell projections that express GAP-43.

Animals↗
PubMed1976

Topical cycloheximide in psoriasis.

Cycloheximide is an antimitotic and an inhibitor of the synthesis of both DNA and protein. Topical application in low concentrations (0.1%-0.2%) resulted in definite involution of psoriatic plaques. Because of its potency this experimental drug - not yet available for clinical use - was employed on small areas only and with extreme caution. Results of a full evaluation for safety, currently in progress, are being awaited with interest.

Administration, Topical↗
PubMed1994

An electron microscopic study of apoptosis induced by cycloheximide in rat liver.

A histological and ultrastructural study, coupled with transmission and scanning electron microscopy of the early changes in the liver following a single administration of cycloheximide (CHX), was carried out in male Wistar rats. At the histological level, apoptosis was already present in the liver 2 h after treatment. By scanning electron microscopy, the following sequential changes were observed: brightness and progressive detachment of hepatocytes from neighbouring cells, formation of surface infolds with multiple blebs and, finally, release of several membrane-bounded apoptotic bodies (ABs) in the extracellular space and into the sinusoidal lumen. Three hours after CHX administration, the apoptotic cycle was completed, as shown by the presence of phagocytosed ABs inside the cytoplasm of intact liver cells. Light microscopic examination of the liver 6 h after CHX administration showed ABs mainly located in the cytoplasm of intact hepatocytes and inside activated Kupffer cells. By transmission electron microscopy, it was possible to demonstrate that cells undergoing apoptosis were hepatocytes. At 24 h, the livers of treated animals appeared normal, with no evidence of apoptosis.

Animals↗
PubMed1988

Interleukin-1 alpha mRNA induced by cycloheximide PMA, and retinoic acid is reduced by dexamethasone in PAM-212 keratinocytes.

Keratinocytes in culture produce detectable amounts of IL-1 alpha mRNA constitutively and can be stimulated to express increased amounts of IL-1 alpha mRNA by cycloheximide, PMA, and retinoic acid. Dexamethasone decreases the amount of IL-1 mRNA induced by these agents, as well as constitutive IL-1 alpha mRNA. RU 486, which interferes with glucocorticosteroid-receptor binding, decreases inhibition of TPA stimulation of IL-1 alpha mRNA by dexamethasone, which suggests that the inhibition by dexamethasone is through a conventional ligand-receptor mechanism.

Animals↗
PubMed1983

Effects of actinomycin D and cycloheximide on the nucleolar ultrastructure of porcine oocytes.

In early antral follicles 0.5 mm in diameter, pig oocytes were intensively engaged in rRNA synthesis. Actinomycin D caused degranulation of their nucleoli which became entirely compact; the fibrillar centers that remained adjacent to the nucleolar surface also increased in size. In contrast, oocytes from preantral follicles treated under the same conditions failed to complete nucleolar compaction and were engaged in a special process of vacuolation. The rate of [3H]-uridine incorporation, evaluated by light-optical autoradiography, indicated that, even at high concentrations, cycloheximide impaired nucleolar transcriptional activity of the oocytes without suppressing it. The nucleoli of such treated oocytes were either unchanged or incompletely transformed, fibrillo-granular regions remaining adjacent to large compact areas. This study provides evidence that the process of nucleolar compaction in pig oocytes depends directly on the inhibition of rRNA synthesis. This process, which only occurs in oocytes from antral follicles, might represent an important step in the acquisition of oocyte capacity to initiate meiotic maturation.

Animals↗
PubMed2006

Cycloheximide protects HepG2 cells from serum withdrawal-induced apoptosis by decreasing p53 and phosphorylated p53 levels.

Cycloheximide (CHX), an inhibitor of protein synthesis, has been reported to prevent cell death in a wide variety of cell types and produced by different apoptotic stimuli. However, the mechanisms by which CHX protects cells from apoptosis are still unclear. In this study, we investigated whether p53 plays a role in the protection by CHX against serum withdrawal-induced apoptosis. Deprivation of serum from the culture medium causes apoptosis in HepG2 cells, and CHX dramatically protects cells from death. p53, p21, and Bax protein levels were elevated, and cell cycle arrest was produced after serum withdrawal. CHX abolished this elevation of p53, p21, and Bax as well as the cell cycle arrest induced by serum deprivation. The p53 inhibitor pifithrin-alpha protects HepG2 cells against apoptosis induced by serum withdrawal. HepG2 cells expressing a dominant negative form of mutant p53 and Hep3B cells lacking p53 were resistant to serum withdrawal-induced apoptosis. Lowering of p53 by small interfering RNA protects HepG2 cells from serum withdrawal-induced apoptosis. p53 phosphorylation was induced by serum withdrawal and other chemotherapeutic reagents such as actinomycin D, doxorubicin, and etoposide. CHX decreases the levels of phosphorylated p53 (pp53) even in the presence of a proteasome inhibitor, which maintains the total p53 levels, whereas it does not affect the dephosphorylation of pp53. These results suggest the possibility that kinases that phosphorylate p53 might be affected by CHX administration. In summary, CHX protects HepG2 cells from serum withdrawal-induced apoptosis through inhibiting the synthesis of p53 and the phosphorylation of p53.

Actins↗
PubMed2004

Identification of cytoskeletal [14C]carboplatin-binding proteins reveals reduced expression and disorganization of actin and filamin in cisplatin-resistant cell lines.

Cisplatin resistant (CP-r) cells often show decreased uptake of cisplatin in association with reduced cell surface proteins and decreased endocytosis. In this report, two major [14C]carboplatin-binding proteins were identified as filamin and actin by photoaffinity labeling and mass spectrometry. Decreased expression of these two proteins was found in two different human CP-r cell lines (KB-CP20 and 7404-CP20), in comparison with their parental cell lines (KB-3-1 and BEL-7404), respectively. Disorganization of beta-actin and filamin 250 and 90 was also detected in these CP-r cells by confocal microscopy. Transfection of a wild-type actin-enhanced green fluorescent protein (EGFP) expression vector into 7404-CP20 cells resulted in a nonfilamentous actin-EGFP distribution compared with a normal distribution in the cisplatin-sensitive BEL-7404 cells, suggesting that cytoskeletal organization is disturbed in the CP-r cells. The identification of actin and filamin as [14C]carboplatin-binding proteins and decreased expression and disorganization of several cytoskeletal proteins in CP-r cells provide a molecular and cellular basis for the known defect in endocytosis in these cells.

Actins↗
PubMed1970

Amnesia produced by electroconvulsive shock or cycloheximide: conditions for recovery.

Retrograde amnesia for a passive avoidance response was produced in rats by electroconvulsive shock and in mice by cycloheximide, an inhibitor of protein synthesis. One day after training the memory could be restored if a "reminder" of the original foot shock was given after the retention test on which the amnesia was demonstrated. Memory did not return if the reminder was given without the prior retention test or if the reminder and the test were separated by 23 hours.

Amnesia↗
PubMed1975

Cycloheximide production by Streptomyces griseus: alleviation of end-product inhibition by dialysis-extraction fermentation.

The use of dialysis fermentation with the continuous extraction of the dialysate has resulted in a twofold increase in the cycloheximide titer due to relief from product inhibition. Continuous extraction of the dialysate has eliminated the necessity for large reservoir volumes of fermentation medium normally used in dialysis fermentation. The apparatus used in this procedure is described.

Cycloheximide↗
PubMed2004

Mechanisms involved in apoptosis of human macrophages induced by lipopolysaccharide from Actinobacillus actinomycetemcomitans in the presence of cycloheximide.

Actinobacillus actinomycetemcomitans is a major periodontopathic bacterium with multiple virulence factors, including lipopolysaccharide (LPS). Previous reports have demonstrated that LPS induced apoptosis in a murine macrophage-like cell line, J744.1, as well as in peritoneal macrophages from C3H/HeN mice in the presence of cycloheximide (CHX). However, the detailed molecular mechanisms involved in the apoptosis of macrophages induced by LPS and CHX are not well known. To clarify the possible role of LPS in the induction of macrophage apoptosis, we investigated cell death induced by LPS from A. actinomycetemcomitans and CHX in human macrophage-like U937 cells, which were differentiated by 12-O-tetradecanoylphorbol 13-acetate (TPA), and also assessed the molecular mechanisms involved in the process. We found that TPA-differentiated U937 cells usually showed resistance to LPS-induced apoptosis. However, in the presence of CHX, LPS induced release of cytochrome c without modifying steady-state levels of Bcl-2, Bcl-xL, Bax, and Bak. Treatment with LPS in the presence of CHX also led to activation of caspase-3 and apoptosis via, in part, the CD14/toll-like receptor 4 (TLR4). The induction of cytochrome c release may have been due to dephosphorylation of Akt and Bad, which were cooperatively induced by CHX and LPS. However, endogenous tumor necrosis factor alpha- and Fas-induced signals, extracellular signal-regulated kinase kinase/mitogen-activated protein kinases and I-kappa B alpha/nuclear factor-kappa B (NF-kappa B) were not required for caspase-3-dependent apoptosis. These results emphasize the possible important role of the mitochondrial apoptotic pathway leading to caspase-3 activation in LPS-induced apoptosis of human macrophages in the presence of CHX.

Aggregatibacter actinomycetemcomitans↗
PubMed1979

Pleiotropic effects of ribosomal mutations for cycloheximide resistance in a double-resistant homocaryon of Neurospora crassa.

Pleiotropic effects of two ribosomal mutations for cycloheximide resistance were studied in a double-resistant homocaryon. The results obtained indicated that the combination of the two ribosomal mutations results in: (i) morphological abnormalities which suggest a severe distortion in the extension of cell walls and membranes; (ii) disturbance in the normal 60S-40S subunit ratio; (iii) decreased rate of cell mass production not necessarily associated with inbalance in the 60S-40S ratio; and (iv) cold sensitivity which does not interfere with mycelial mass production.

Cold Temperature↗
PubMed1995

Inducible expression of a gene encoding an L41 ribosomal protein responsible for the cycloheximide-resistant phenotype in the yeast Candida maltosa.

In a previous paper (S. Kawai, S. Murao, M. Mochizuki, I. Shibuya, K. Yano, and M. Takagi, J. Bacteriol. 174:254-262, 1992), we showed that in each genome of several yeast species, there is one of two types of L41 gene, one for an L41 (Q-type) protein which confers cycloheximide (CYH) resistance or one for an L41 (P-type) protein which does not. These genes have been suggested to be responsible for the CYH response used in taxonomy. For example, Saccharomyces cerevisiae, which is CYH sensitive, has a P-type L41 gene, while Kluyveromyces fragilis and Candida maltosa, which are CYH resistant, have Q-type L41 genes. However, in contrast to K. fragilis, which is constitutively resistant to CYH, C. maltosa is inducibly resistant to CYH. Here, we show that C. maltosa has both types of the L41 gene in its genome and that expression of the Q-type L41 gene is induced by CYH while the P-type L41 gene is constitutively expressed.

Base Sequence↗